Abstract
Evidence is accumulating that implicates neuropeptides, substance P (SP) in particular, in early pathogenetic mechanisms of rheumatoid arthritis and other arthritides. Kinins, prostaglandins, oxygen radicals and other substances lower the activation threshold of peripheral unmyelinated afferent bres (sensitisation). These bres release in ammatory mediators, such as leukotrienes, which in turn stimulate lymphocytes and synovial proliferation and induce release of interleukin-1, tumor necrosis factor and interleukin-6 from monocytes. Also, these substances can sensitise or even excite nociceptors. All the mentioned factors produced by nerves or by other cells are key factors for the pathologic alterations observed in chronic and acute arthritides.
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